PHARYNGITIS (TONSILLOPHARYNGITIS)

PRINCIPLES OF DISEASE Pathophysiology

Inflammatory syndrom of the oropharnx primarily caused by infection Transmission usually through respiratory secretions, but fomite, food

transmission also possible Infection localizes in lymphatic tissue: tonsils, cervical ln.s Rare significant complications of airway obstruction, decreased oral intake

and dehydration Chronic pharyngitis: inflammation and infection of the tonsillar crypts

rather than the tonsils themselves Beta-lactamase production is extremely common in bacteria responsible

for chronic pahryngitis Microbiology

Viral most common cause: 80 - 90%; rhinovirus, adenovirus, coronavirus, CMV, parainfluenza, rubella, influenza, HSV, coxsachie, EBV

Bacterial (children): group A Beta-hemolytic Streptococcus (GAS) (Streptococcus pyogenes)

Bacterial (adults): Beta-hemolytic strep (all groups), H.flu, Mycoplasma, Chlamydia

Other causes: Actinomyces, Francissella tularenssi, Yersinia enterocolitica, Group B, C, G Streptococci

Cultures: often mixed aerobes (staph aureus, Hflu, moraxella) and anaerobes (bactroides, anaerobic gram + cocci, fusobaclterium)

CLINICAL FEATURES Hx:pharyngeal pain and odynophagia PE: pharyngeal erythema, pharyngeal or tonsillar exudate, tonsillar enlargement, tender

cervical lymphadenopathy Strawberry tongue: petecheiae or hemorrhagic lesions suggesting scarlet fever Gingival lesions with ulcerating tonsillitis and pseudomembranous exudate: Vincent’s

angina Bull neck: diptheria Vesicles: HSV, coxxachie Rash: sand-papery with scarlet fever, erythematous maculopapular with EBV Clinical differentiation of etiology is virtually impossible; some clues

Viral: associated rhinitis, cough, myalgia, headache, stomatitis, conjunctivitis, exanhem, odynophagia, low-grade fever, white exudate; cervical lymphadenopathy less common

Bacterial: rhinitis, conjuctivitis, exanthem, lymphadenopathy less common; exudate, high fever, cervical lymphadenompathy, abscence of cough more common

VIRAL PATHOGENS Systemic viral infections: measles, CMV, rubella, HIV (mono-like illness) Influenza: fever, headache, myalgias; 50% with pharyngeal pain but minority with

exudate and cervical lymphadenopathy Adenovirus: 30% associated with conjunctivitis

Mononucleosis: pharyngitis is common presentation, tonsillar exudate or membrane (creamy or cheesy whit), generalized lymphadenopathy in 90%, splenomegaly in 50%, periorbital edema and rash less common. Macular rash after amoxicillin is common (90% of those with mono given amoxil)

HSV pharyngitis: young adults, painful superficial vesicles on erythematous base, ulcers may be present on lips/pharyng/tongue/gingiva/buccal mucosa, pharyngeal erythema and exudate + fever + ln.s for 1-2 weeks, can be primary or secondary, bacterial superinfection a complication

BACTERIAL PATHOGENS Group A Beta-Hemolytic Streptococcus

primarily 5 - 15, winter and spring, incubation 12hr - 4 days < 15% of pharyngitis in > 15yo, rare < 3 yo, epidemics occur fever > 38.3, tonsillar exudates, palatal and uvular petechiae, uvular

edema and erythema, tender anterior cervical ln.s, absence of cough/rhinitis.

Rash: associated with diffuse erythematous fine sandpaper rash, first in flexor areas then generalized, concentrated in axilla, inguinal, popliteal fossa; characteristically FADES on pressure; lasts 7 days then desquamates (scarlet fever); not sensitive or specific; due to pyrogenic toxin; occurs in minority

Pastia’s lines: petechiae in folds of the joints Strawberry tongue can occur with scarlet fever Toxic shock syndrome: sepsis and cardiovascular collapse, < 1%,

pyrogenic exotoxin A, high mortality Diptheria

uncommon b/c of vaccinations, potentially lethal, consider in immigrants sore throat, fever, dysphagia, gray or white exudate that coalesce to form

a pseudomembrane which is a gray-green layer over the tonsils, pharyngeal mucosa, and occassionally the uvula and may extend to involve the larynx (hoarseness, cough, stridor)

severe inflammation and edema can produce dysphonia and a “bull-neck”appearance

laryngeal, nasal, and cutaneous involvement possible (sharply demarcated ulcer with membranous base)

must ask for special culture medium Corynebacterium diptheriae produces a systemic toxin ----> myocarditis,

arrythmias, polyneuritis, vascular collapse, organ necrosis, death Arcanobacterium hemolyticum

previously called Corynebacterium hemolyticum, 10 - 30 year old similar to GAS pharyngitis, most have rash scarlatiniform/urticarial/or

erythema multiforme (may be only complaint) usually nontoxic and afebrile; can produce membrane similar to diptheria;

associated with chronic pharyngitis

Vincent’s angina anaerobic pharyngitis and acute necrotizing ulcerative gingivitis (ANUG) also called Trench Mouth etiology: Borellia vincenti superficial ulceration and necrosis that often results in the formation of a

pseudomembrane and gingival lesions

food deposits in gingival crevice, gingivitis, frank ulceration and bleeding, pseudomembranous necrotic exudate in gingival margins, spread to tonsils and pharynx

foul-smelling breath, odynophadia, submandibular lymphadenopathy, exudate often present, poor oral hygiene common

Gonococcal pharyngitis STD, may be independent of genital infection, can be asymptomatic

carrier, latent period common, important cause of gonococcemia Syphillitic pharyngitis

primary or tertiary syphillus, painless mucosal lesions Tuberculosis pharyngitis

hoarseness, dysphagia, pharyngeal ulcers in patient with advanced disease

Candidal pharyngtitis dysphagia, odynophagia, adherent white plaques with focal bleeding

points, immunocompromised Mycoplasma pneumoniae

mild pharyngitis, epidemics occur, up to 10% of all adult pharyngitis, may have LRTI as well

Chlamydia pneumoniae epidemics, severe, selling and pain of deep cervical lymph nodes, +/-

LRTI, hallmarks are recurrence and persistence Chlamydia trachomatis

STD, urogenital and partner testing required, mild symptoms or asymptomatic

DIFFERENTIAL DIAGNOSIS Deep space infections, Tumors, Foreign bodies Pemphigus, Steven Johnson syndrome, Drug reaction Allergic reaction, Angioedema Chemical and thermal burns Esophagitis, GERD Epiglotitis, thyroiditis DIAGNOSTIC STRATEGIES Mononucleosis

Monospot: 95% sensitive in adults, 90% sensitive in > 5yo, 75% sensitive in 2 - 4yo, 30% sensitive in 0 - 2yo; commonly negative in first week of illness; specificity can be a concern as test may remain positive for up to a year following the illness; POOR in young and early in dz

EBV IgM antibodies can be measured EBV nuclear antigens develp w/i 3-6weeks and can be useful if initial

testing is negative Peripheral blood smear reveals atypical mononuclear cells in 75% with

peak incidence in 2nd to 3rd week of illness Group A Beta-Hemolytic Strep

Important to diagnose and treat w/ abx to prevent rheumatic fever Antibiotic do NOT prevent post - strep glomerulonephritis Difficult to dx or r/o accurately with clinical assessment Serology: Anti-Streptolysin O (ASO) titers acute and convelescent are only

reliable way to diagnose; looks for grp A only; very specific but sensitivity is variable (60 - 90%)

Throat swab cultures 90 - 95% sensitive for detection of Streptococcus pyogenes but specificity (50%) may be poor as asymptomatic carriage is common; lab only looks for GAS, must ask for diptheria etc

Rapid diagnostic tests: latex agglutination, ELISA, optical immunoassay, chemiluminescent DNA probes; looks for streptococcal antigen in the throat swab (only grp A); sensitivities range from 30 - 100% and specificities range from 70 - 100% in trials but lower in practice; use is controversial considering significant false +ve and false -ves

Clinical scoring system­ fever > 38.3­ cervical lymphadenopathy­ tonsillar exudate­ absence of cough

Other testing Diptheria: requires specific culturet, toxigenicity testing must also be

performed A. hemolyticum: suspect if rash present, including EM Vincent’s angina: clinical suspicion and a gram stain Gonococcus: requires a Thayer-Martin agar TB: requires acid-fast staining Syphilus: dark-field microscopy, direct immunofluorescence, serology Candida: yeast on KOH prep of throat swab or Sabouraud’s agar Mycoplasma: serology or culture Chlamydia: serology or antigen detection tests HSV: culture of vesicles

MANAGEMENT Group A Beta-hemolytic Strep

Clinical judgement unreliable, poor diagnostic tests, vastly overtreated Benefit of antibiotics: shorten course of illness by < 1 day (2or3 vs 3or4),

decreases transmission, prevention of complications, decrease incidence of rheumatic fever (or is a change in strain pattern, because rheumatic fever rarely seen today compared to 50 years ago, is it really the antibiotic use?)

Disadvantage of antibiotics: increased bacterial resistance, increased recurrence, decreased immune response, patient expectation of abx

Rheumatic Fever: treatment w/i 9 days will prevent RF, incidence dramatically decreased after antibiotic use, peak incidence in 5 - 15yo where Grp A Beta - hemolytic strep common, currently occurs in 0.3% of GAS pharyngitis and may increase to 3% with epidemics

Tonsillectomy: > 5 episodes per year Antibiotics does NOT prevent post-strep glomerulonephritis Four ED strategies

­ throat culture all and only treat positives: costly, poor specificity of positive culture b/c of carriage rate, delay in waiting for cultures, problems with f/u from ED,

­ treat all, culture all, stop if culture negative: ineffective and costly

­ perform rapid strep test and treat those who are positive:

false +ve lead to over treatment, negative test requires follow up cultures,

­ treat all who have reasonable clinical probabililty of GAS: leads to over-treatment but avoids problems with testing

­ COMBINATION: high clinical probability should be treated without testing, low clinical probability should be treated if testing is positive (culture or rapid strep testing)

Group A Beta-hemolytic Strep antibiotic regimen­ Penicillin V 250 mg po qid X 10days­ Penicillin V 250 mg po qid X 2/7 then 500 mg bid X 8/7­ Benzathine Penicillin 1.2 million units im X 1 dose­ Frequent dosing necessary, im dose has more reactions­ Erythromycin 500 mg bid X 10/7 for pen allergic­ Penicillin failure due to noncompliance, re-infection, or Beta

- lactamase production; penicillin resistance growing, erythromycin resistance uncommon

­ Alternatives: cephalosporins, macrolads, clindamycin (not shown to prevent RF although probably do)

­ Amoxicillin, ampicillin, and penicillinase - resistant penicillins offer no advantage over uncomplicated GAS infections

Other Bugs Diptheria: concern for toxicity and airway compromise; treat immediately if

suspecting, don’t wait for tests; equine ANTITOXIN is indicated based on clinical grounds, dose varies, consultation required; antibiotics eradicate the bug but not the toxin, use erythromycin or rifampin; Td booster for immunized contacts and erythromycin + full vaccination course for unimmunized contacts

A. hemolyticum: erythromycin d of c b/c of penicillin resistance Vincent’s angina: penicillin or clindamyucin and aoral oxidizing agent

(hydrogen peroxide) Gonoccocus: ceftriazone 125 mg im or cipro/cifixime single dose;

concomitant treatment with azithromycin or doxy to cover chlamydia TB: multiple drug regimen Syphillus: benzthine penicillin 2.4 million units or doxycycline X 14 days Candida: nystatin swish and swallow, versus oral

GAS CLINICAL SCORING SYSTEM

(i) fever > 38.3 (ii) cervical ln.s (iii) tonsillar exudate (iv) NO cough

0 - 1: no treatment or testing2 - 3 : test, treat if positive

4: treat empirically

fluconazole/itraconazole/clotirmazole; chronic suppression with HIV Mycoplasma pneumonia: erythromycin, doxycycline, tetracycline Chlamydial: doxy or macrolide Recurrent tonsillitis: B-lactamase resistent antibiotics HSV: acyclovir X 1 week if primary infection Steroids? Mayshorten the duration of symptoms without increasing the

complication rates Symptomatic

Tylenol, ibuprofen Warmed fluids, topical anesthetics (cepacol, etc)

Mononucleosis Supportive, hydration, consider steroids Avoid sports or contact for 6-8 weeks (risk of splenic rupture) Acyclovir or famiciclovir if immunocompromized

DISPOSITION Complications may necessitate consultation and admission: Airway compromise, Local

and distant spread of infection, Deep neck abscesses, Necrotizing fascitis, Sleep apnea, Bacteremia/sepsis

Complications of mono: airway obstruction, tonsillar and peritonsillar abscess, lingual tonsillitis, necrotic epiglottitis, hepatic dysfunction, splenic rupture, neurologic disorders, pneumonitis, pericarditis, hematologic disorders

GAS complications Suppurative: PTA, RPA, deep space abcessess, suppurative cervical

lymphadenitis, OM, sinusitis, mastoidtits, bacteremia, sepsis, OM, meningitis,

Nonsuppurative: RF, GN, pericarditis, myocarditis, erythema nodosum, streptococcal toxic shock syndrome

­ Rheumatic Fever: rare, 18 days after infection is average, carditis and secondary valve disease, certain serotypes more of a problem (with M-protein), prevented with abx w/i 9 days

­ Glomerulonephritis: uncommon, 10 days after infection is average, usually nephritic syndrome, uncommon progression to CRF, serotype M-type 12, NOT prevented by abx

ADULT EPIGLOTTIS

PRINICPLES OF DISEASE Potentially life-threatening condition from airway obstruction Increased incidence and recognition in adults; uncommon in peds after Hflu vaccine Localized cellulitis of upper airway Marked involvement of the supraglottic structuress: base of tongue, vallecular,

aryepiglottic folds, arytenoid soft tissues, lingual tonsils, epiglotis Inflammation does NOT extend to the infraglottic rections b/c the submucosa is so

densely adherent to the mucosa below the vocal cords Supraglossitis: reports of severe supraglottic involvement with normal epiglottis H. influenza type B is most common isolate

Majority have NO organisms identified by blood or supraglottic cultures ? viral (adenoviral) role

CLINICAL FEATURES No age, seasonal prevelance Males, smokers more commonly affected Prodrome variable: hours - days Rapid progression is predictor of airway compromise Sore throat, odynophagia, dysphagia (pain severe), STRIDOR Dysphonia and muffled voice common; usually NOT hoarse Fever in 50% and late Tacchycardia out of proportion to fever Tenderness over anterior neck in hyoid region and on moving larynx are reliable Imminent airway obstruction: stridor, drooling, respiratory distress, sniffing position Pharyngeal examination does not r/o epiglottis b/c of concominant pharyngitis, uvulitis,

tonsillitis, Ludwig’s angina, PTA, parotitis

DIAGNOSIS Differential diagnosis

Misdiagnosis common: strep pharyngitis is most common misdiagnosis Monon, deep space infections, lingual tonsillitis, diptheria, pertussis,

croup, angioedema, allergy, FB, laryngospasm, tumor, toxic inhalant, aspiration, laryngeal trauma

Laryngoscopy Direct, indirect, or fiberoptic visualization if not in respiratory distress Swollen epiglottis and surrounding structures, epiglottis may be “cherry

red” but often is pale and edematous Respiratory distress, stridor, drooling, aphonia: indirect laryngoscopy

contraindicated and direct laryngoscopy only if prepared for airway Lateral soft tissue of neck

Sensitivity 80 - 90% (does NOT rule out) Xrays: obliteration of vallecula, swellin of arytenoids and aryepiglottic

folds, edema of prevertebral and retropharyngeal soft tissues, “ballooning”of the hypopharynx and mesopharynx, edematous thumb shaped epiglottis (Epiglottis > 8mm or Aryepiglottic fold > 7mm)

Direct laryngoscopy indicated if suspecting and Xrays normalMANAGEMENT Expect sudden, unpredictable airway obstruction Minimize stimulation, have airway equipment by the bed, have cric tray at bedside, notify

OR and consult ENT emergently if airway compromise present or expected Hands off and transfer to OR for definitive airway management if at all possible If airway obstructs in ED: try orotracheal, could try LMA, be set up and ready for TTV or

cricothyrotomy Safety and efficacy of Orotracheal and laryngoscopic guided nasotracheal intubation

reported Blind nasotracheal intubation may lead to airway obstruction and is contraindicated Lateral neck Xray (portable) may be helpful but don’t waste time to OR Start antibiotics ASAP: cefuroxime, ceftriaxone, cefotaxime ? role for steroids and racemic epinephrine Disposition

Mild cases: mild swelling on laryngoscopy without drooling, stridor, or respiratory distress --------> ICU for treatment and monitoring without intubation

Moderate/Severe: to OR for intubation, to ICU So who needs intubation? Alert, stable, not tiring, no resp distress can be

monitored Complications

Meningitis, RPA, pneumothorax, empyema, pneumonia, sepsis, ARDS, pulmonary edema

DEEP SPACE INFECTIONS OF THE LOWER FACE AND NECK

Deep space infection of neck are dangerous and require rapid treatment Much less common because of dental hygeine and antibiotics Distorted airway anatomy = difficult airway Paralytics may cause muscular laxity and worsen the degree of airway obstruction Fiberoptic intubation useful BNI can cause abscess rupture, airway damage, further compromise Submandibular space: conglomerate of the sublingual and submaxillary spaces which

clinically function as a single space Sumandibular space is involved in Ludwig’s angina Five clinically relevant potential spaces in neck (figure 70-4)

Peritonsillar space Parapharyngeal space: carotid, jugular vein, CN IX –> XII, sympathetics Retropharyngeal space: lies in the midline, medial to the parapharyngeal

space and extends from the base of the skull to the superior mediastinum at the level of T2; superior constrictor muscle adheres to the prevertebral fascia and forms a raphe in the medial aspect ot the retropharyngeal space :. retropharyngeal abscesses tend to occur lateral to the midline

Danger space: base of the skull to the diaphragm: abscesses will be midline

Prevertebral space: base of the skull to the coccyx: abcesses will be midline

Retropharyngeal, danger space, and prevertebral space infections have easy access to mediastinum, Danger space, Prevertebral space which all communicate

Rapid spread of infection occurs easily through facial planes and spaces

PERITONSILLAR CELLULITIS (PTC)AND PERITONSILLAR ABSCESS (PTA)

PRINCIPLES OF DISEASE PTC and PTA are a continuum of peritonsillitis PTA (quinsy) is the most common deep infection of the adult head and neck Result of acute tonsillitis: infection of weber’s glands or tonsillar crypts invades the

peritonsillar tissues leading to cellulitis that may progress to abscess formation Fibrous fascial septae divide the peritonsilar space into compartments and direct the

infection anteriorly and superiorly Risk factors: chronic tonsillitis, mono, smoking, CLL, tonsilloliths, dental infection All age groups, CAN occur with previous tonsillectomy, recurrence in up to 50% Polymicrobial aerobes (GAS, strep milleri, Hflu, strep viridans) and anaerobes

(fusobacterium, bacteroides, peptostreptococcus, actinomyces)

CLINICAL FEATURES Odynophagia, dysphagia, drooling, trismus, referred otalgia, muffled “hot potato” voice,

rancid breath, systemic symptoms of fever, dehydration, malaaise Recurrent tonsillitis hx common PE: trismus, inflammed and erythematous oral mucosa in peritonsillar area, purulent

tonsillar exudates that may cover the tonsil, tender cervical lymph nodes PTC versus PTA can be difficult

TRISMUS and UVULAR DEVIATION are the best predictors of abscess versus cellulitis

DIAGNOSIS Clinical diagnosis for PTC Aspiration of pus for PTA Mono common (20%) and monospot testing may be relevant Xrays of limited utility Contrast CT, intraoral ultrasound, transcutaneous ultrasound useful when patients

unable to co-operate with needle aspiration PTA needle aspiration

Adv: diagnostic and therapeutic, easy and safe in ED, minimal pain compared to surgical incision and drainage

Disadv: difficult if uncooperative or children, may miss abscess and lead to misdiagnosis of PTC, greater recurrence of PTA c/p to I&D, carotid artery puncture theoretical (NO case reports in literature)

Differential diagnosis Hypertrophic tonsillitis, mono, diptheria, deep space infections of neck,

cervica adenitis, congenital or traumatic internal carotid artery aneuryms, foreign bodies, neoplasms

MANAGEMENT No suspicious findings for abscess = suspect Peritonsillar Cellulitis

Don’t attempt ED aspiration IV antibiotics and f/u with HPTP

Suspected Peritonsillar Abcess Needle aspiration in ED (except in peds) Start IV abx F/U with HPTP Arrange ENT follow up

Controversies Aspiration equivalent to I&D in three small studies

Indications for tonsillectomy: two PTAs, septic, etc Do all need to see ENT? recurrent, large, can’t aspirate in ED Which antibiotic?

­ Ancef + flagyl­ Ceftriaxone + flagyl­ Pencillin + flagyl­ Clindamycin alone (general choice in peds)

IV antibiotics and observation before surgical intervention an option Complications

Airway obstruction is most important complication Other: abscess rupture with aspiration, pneumonia, empyema, pulmonary

abcess, prapharyngeal and retropharyngeal spread of infection, Ludwig’s angina, mediastinitis, myocarditis, carotid artery erosion, jugular vein thrombophlebitis, septic embolization, postanginal septicemia (Lemierre’s syndrome) and cervicothoracic necrotizing fascitis

Intracranial: meningitis, venous sinus thrombosis, cerebral abscess Systemic: dehydration, sepsis, toxic shock

Dispostion Admission: dehydration, inability to tolerate po intake, toxic, underlying

diseases, severe pain, complications Discharge: generally iv abx through outpatient iv program

RETROPHARYNGEAL (RPA) AND PREVERTEBRAL SPACE ABSCESSES

PRINCIPLES OF DISEASE Retropharyngeal swelling occurs from expansion of either the retropharyngeal space,

danger space, or the prevertebral space (figure 70-4) -----------> collectively described as retropharyngeal abscesses (RPA)

Previously a childhood disease, but increasing adult incidence Children < 4yo have prominent retropharyngeal lymph nodes that become infected, lead

to retropharyngeal cellulitis and RPA formation Retropharyngeal nodes atrophy after 4 - 6 yo and thus decreasing incidence and

different pathology in adults Adults: cellulitis in retropharyngeal area and abscess may form; nasopharyngitis, OM,

parotitis, tonsillitis, PTA, dental infections and procedures, upper airway instrumentation, Ludwig’s angina, lateral pharyngeal space infection, endoscopy are all implicated as causes

Blunt and penetrating trauma also causes: FB, fish bones, cautic ingestion, vertebral fracture

Hematologic spread less common Diabetes and immunocompromised states may be important Polymicrobial aerobes and anaerobes is most common Vertebral osteomyelitis leading to RPA is most commonly staph Tuberculosis was a common cause, but not now

CLINICAL FEATURES Sore throat, odynophagia, dysphagia, drooling, muffled voice, neck stiffness, neck pain,

fever Dysphonia described as a duck “quack” (cri du canard) May be toxic, airway obstruction and respiratory distress possible Sniffing position to protect airway can occur May have posterior neck or shoulder pain with swallowing Physical Examination

Tender cervical ln.s, tender cervical musculature, neck swelling, torticollis, high fever, trismus may be present

Diffuse edema/erythema of posterior pharynx with retropharyngeal cellulitis

Palpation of abscess: unreliable, risk of rupture Visualization of abscess: midline lump with prevertebral or danger space

and unilateral if retropharyngeal space Tenderness on moving the larynx and trachea side to side (tracheal rock

sign)

DIAGNOSIS Lateral neck Xray

Inspiratory film with widening of retropharyngeal space and forward displacement of esophagus and trachea

Diffuse swelling with cellulitis, more localized with abcess Xrays are unreliable to distinguish RP cellulitis versus RP abscess Other: loss of cervical lordosis, air-fluid level in abcess, FB, vertebral body

destruction (AIR in RP space is good predictor of abscess) Retropharyngeal space > 7mm at level of C2 is abnormal in kids and

adults Retropharyngeal space > 14mm adults and 21mm kids at level of C6

Other CXR to evaluate mediastinal involvement CT or MR good for detection of complications CT with iv contrast is considered the “gold standard” for diagnosis but

studies show sensitivity 90 - 100% and specificity 60 - 70 % (low) for RPA vs RPC

U/S useful tod etect RPC from RPA Differential Dx

Cold abscesses: tuberculosis; insidious onset, chronic, constitutional symptoms, minimal fever, symptoms >> physical findings

RP tumors, FB, hematoma, aneurysm, hemorrhage, lympadenopathy, edema, retropharyngeal thyroid tissue, tendinitis of longus colli muscle

MANAGEMENT RPC: iv antibiotics, choices as per Ludwig’s angina, consider TB and fungal RPA: surgical incision and drainage, iv antibiotics (may try abx X 48hr before surgery) Cold abscesses: drained extraorally, unless in acute distres Vertebral body destruction: neck immobilization could be necessary with vertebra

osteomyelitis or atlantoaxial separation; external fixation possibly required Complications: abscess rupture and aspiration, pneumonia, empyema; extension to

mediastinum, pericarditis, pleuritis, empyema; vascular erosion; atraumatic atlantoaxial separation due to damage of transverse ligament of atlas (wide predental space on Xray or CT); acute transverse myelitis, epidural abcess; esophageal erosion, necrotizing fascitis, ARDS, sepsis

Disposition Admitted, consultation with ENT, surgical intervention

PARAPHARYNGEAL ABSCESS (PPA)PRINICPLES OF DISEASE Parapharyngeal space (lateral pharyngeal space, pharyngomaxillary space) divided into

two compartements by the styloid process Anterior compartment: muscle, lymph nodes, connective tissue Posterior compartment: carotid sheath (carotid artery, internal jugular vein,

vagus nerve, CNIX/X/XI/XII, cervical sympathetic chain) Etiology: dental infections, pharyngotonsillary infections are most common causes Other causes: spread from surrounding deep spaces, parotits, sinusitis, neck tumors,

infected branchial cleft cysts, mastoiditis, suppuration of local lymphadenitis, iatrogenic introduction by anesthetic blocks/tonsillectomy/nasal intubation/dental work

Polymicrobial

CLINICAL FEATURES Pain and swelling of the neck, odynophagia, dysphagia Classic: medial tonsillar displacement and posterolateral pharyngeal wall bulge Other findings: fever, trismus, edema, swelling at angle of jaw, erythematous/tender/and

nonfluctuant mass at angle of mandible Diagnosis

Clinically diagnosis Lateral neck Xray: upper prevertebral soft tissue swelling, otherwise not

helpful U/S, CT, MR useful Ddx: as per RPA

MANAGEMENT ENT consultation IV antibiotics as per Ludwig’s angina Surgical drainage

COMPLICATIONS AWO, rupture, aspiratoin, pneumonia, empyema, mediastinitis, necrotizing fascitis,

bacteremia, sepsis, pericarditis, osteomyelitis of mandible, parotid abcess, cavernous sinus thrombosis, meningitis

Unique complication of posterior pharyngeal infections Cervical sympathetic chain: horner’s Carotid artery erosion and aneurysms: oral, nasal, aural warning bleeding

is common; unexplained bleeding with H/N infections is serious and

warrants aggressive investigation, persistent peritonsillar swelling and unilateral tender pulsatile masses may be clues

CN IX —> XII palsies

“Lemierre’s syndrome” (also called postanginal septicemia): IJ thrombophl Young, healthy patients, pharyngitis that improves then followed by severe

sepsis, confused with right sided endocarditis or aspiration pneumonia Pharyngeal infection spreads to the paraphyngeal space and causes

septic thrombophlebitis of the jugular vein Metastatic infectious spread to lungs cause bilateral nodular infiltrates,

pleural effusion, pneumothoraces Septic arthritis, osteomyelitis, meningitis, vesiculopustular rash are also

reported result of septic embolization Leukocytosis, incr bilirubin, incr LFTs, hematuria, renal failure, all reported Full septic picture with its complications reported Fusobacterium and Staph aureus are most common causes Antibiotics +/- jugular vein ligation and resection

LUDWIG’S ANGINAPRINCIPLES OF DISEASE Progressive cellulitis of the connective tissues of the floor of the mouth and neck that

begins in the submandibular space Potentially fulminant, death within hours is possible Dental disease is the MCC: infected or recently extracted tooth in almost all cases Lower 2nd and 3rd molars are the MC teeth afftected Dentoalveolar abscesses may easily break through the relatively thin cortex of the

mandible below the mylohyoid ridge and infect the submandibular spaace Other causes: mandible fracture, FB or laceration to floor of the mouth, tongue piercing,

traumatic intubation/bronch, oral Ca that gets infected, OM, submandibular sialoadenitis, PTA, furuncle, infected thyroglossal cyst, sepsis

Polymicrobial: aerobes/anaerobes (staph, strep, bactroides, pseudomonas, klebsiella, candida)

CLINICAL FEATURES Sublingual and submaxillary space infections leads to edema and soft tissue

displacement which may result in airway obstruction Symptoms: dysphagia, neck swelling, neck pain, dysphonia (“hot-potato”), odynophagia,

dysarthria, drooling, tongue swelling, pain in floor of mouth, restricted neck movement, sore throat, history of dental extractions/dental pain, foul taste in mouth; air release, creptius, unilateral pharyngitis in any one with recent dental extraction is a clue

PE: bilateral submandibular swelling and elevation or protrusion of the tongue, elevation of the floor of the mouth, posterior displacement of the tongue, “woody”consistency of the floor of the mouth, tense edema and brawny induration of the neck above the hyoid (“bull neck”), marked tenderness of neck, subQ emphysema of neck, trismus, fever, cervical LN, percussion tenderness over teeth

DIAGNOSIS Five diagnostic criteria

Cellulitis with little or no pus present in the submandibular space Bilateral cellulitis Gangrene present with serosanguinous, putrid fluid Connnective tissue, fascia, muscle involvement but glandular tissue

spared Cellulitis spread by continuity and not by lymphatic vessels

Investigations Lab not very helpful Fluid for culture and gram stain Xrays: swelling of affected area, gas collections, panorex may

demonstrate periodontal abscess and other dz Ultrasound: cellulitis versus abscess

Differential Dx Deep cervical node suppuration, PTA, other deep neck abscesses,

parotid abscess, submandibular gland abscess, oral cancer, angioedema, submandibular hematoma, laryngeal diptheria

MANAGEMENT Airway

Airway obstruction and asphyxiation is the MCC of death Airway may obstruct rapidly Continuous monitoring essential Stridor, tachypnea, dyspnea, inability to handle secretions are indicators

of impending airway obstruction Fiberoptic nasotracheal intubation is the preferred method of intubation

Definitive therapy Antibiotics: high dose penicillin + flagyl or ptip-tazo or clinda Steroids: unknown role Surgery: incision and drainage if failure of antibiotics, crepitus and

purulent collections Dental extraction

Complications Spread of infection: deep spaces of neck, empyema, mediastinitis,

mediastinal abscess, pericarditis, aspiration pneumonia, lung abscess IJ thrombosis, carotid artery erosion, bacteremia, sepsis, subphrenic

abscess, necrotizing fascitis, spontaneous pneumothorax Disposition

Admission, iv abx, ENT consult, +/- ICU monitoring

SINUSITISPRINCIPLES OF DISEASE Definition: inflammation of one or more of paranasal sinuses; acute < 4/52, chronic> 3/12 Common, viral URTIs complicated by sinusitis in 0.5 - 2.0% Viral sinusitis 200Xs more common than bacterial sinusitis Pranasal sinuses: frontal, maxillary, ethmoid, sphenoid based on which bone they are in Maxillary sinus: triangular, base being the lateral nasal wall and apex extending into the

zygoma Ethmoid: anterior and posterior, 2 - 8 anterior air cells and 1 - 8 posterior air celss Ethmoid: blood supply connects tot eh opthalmic vessels and cavernous sinus;

dangerous re spread tot eh orbit or CNS Frontal: variable pneumatization from aplastic to extensive; bony septum between left

and right; Sphenoid: bony septum, optic nerve and carotied artery occupy the lateral walls of the

sphenoid sinus Ethmoid and maxillary sinuses are present at birth Sphenoid sinuses start to develop at 2yrs and not well developed until 6 yrs - 12 yrs Frontal sinuses start to develop at 2 yrs, are small until 6 years, not full developed until

teens Medial meatus: drainage for the maxillary, anterior ethmoid, frontal sinuses; located b/w

the inferior and middle turbinates; this area is the ostiomeatal complex and is the focal point of sinus disease

Superior meatus: drainage for the posterior ethmoid Sphenoid sinus drains just above th superior turbinate Healthy sinus depends on patent ostia with free air exchange and mucus drainage so

that it does not accumulate mucus and remains sterile. URTI and allergic rhinits are the MCC of ostial obstuction with resultant sinusitis

Ciliary abnormalities are also important: URTI, genetic syndromes Compromised drainage leads to resorption of air, lowers oxygen tension, increased

metabolism, lowers the pH, bacterial introduction by coughing or blowing nose, inflammation and bacterial overgrowth

Allergic sinusitis: sneezing, itchy eyes, allergen exposure, prior episodes Viral sinusitis up to 200Xs more common than bacterial Bacterial pathogens: pneumococcus, Hflu (50% together), Moraxella catarrhalis (10%)

are primary bacteria; anaerobes, streptococcal species, staph aureus more important in chronic sinusitis (polymicrobial often associated with dental disease); pseudomonas (HIV and CF)

Immunocompromised: aspergillus, candida, histoplasma, blastomyces, coccidioides, cryptococcus, rhizopus, etc (especially with DKA)

Mucormyocosis Invasive, aggresive fungal sinusitis in the Immunocompromised Fever, localized nsal pain, cloudy rhinorrhea, grey/friable/anesthetic

terbinates that do not bleed because of angioinvasion (may be necrotic and black tissue)

Risk Factors Medical conditions: resp infections, allergic rhinitis, CF, immunodeficiency,

Wegener’s syndrome, Kartagener’s syndrome Irritants: smoke, polution, chorine, cocaine Anatomy: deviated septum, adnoidal hypertrophy, immotile cilia, polpys,

tumors, foreign bodies, NG tubes Trauma: facial fractures, dental procedures, diving

CLINICAL FEATURES Symptoms

Worsening symptoms after 5 days or persistent after 10 days Double sickening: cold who improves initially only to have worsening sinus

congestion and discomfort Nnasal congestion, nasal obstruction,mucopurulent discharge, post-nasal drip that may lead to cough, pressure/pain over the involved sinus, malaise, fever

Pain over the affected sinus is the main symptom Sphenoid sinus: vague bitemporal h/a or various focal points anywhere in

head Maxillary sinusitis: pain over the zygoma, canine or bicuspids, or

periorbitally Ethmoid sinusitis: medial canthal pain and periorbital or temporal

headache Chronic Sinusitis: slow onset, prolonged duration, recurrence; symptoms

similar to acute but may also have cough, fetid breath, laryngitis, bronchitis, worsening asthma

Pediatric sinusitis symptoms: more nonspecific; persitant URTI X 10 - 14 days with persistent nasal discharge and continued unwell state (+/- fever, irritabiliby, lethargy, cough, poor feeding) -----> consider foreign bodies, asthma, tumors, polyps, CF

Physical Examination Periorbital edema or other facial swelling Tenderness by palpation or percussion over the maxillary or frontal sinus

(no way to palpate the ethmoid or sphenoid sinuses) Maxillary teeth tenderness (10% related to dental infection) Malodorous breath in absence of other cause Anterior rhinoscopy (est performed after application of topical

decongestant)­ Erythema and edema­ Mucopurulent discharge in nose­ Mucopurulent discharge from middle meatus or sinus ostia­ Anatomic anomalies (polyps, deviated septum)

Transillumination How: dark room, light against infraorbital rim and look in pt mouth to see

how much light is transmitted through maxilla (or can put light in mouth); place at supraorbital rim and aim toward frontal sinus

Only 55% of patients with findings on CT have findings on transillumination and CT is nonspecific :. transillumination is not sensitive

Interobserver reliability 60% Questionable role in adults No role in kids < 9 b/c thick bone and soft tissues, different rates of sinus

development b/w kids and b/w sides, lack of aeration of sinuses

RADIOLOGY Plain films

What to look for: sinus opacification, air - fluid level (insensitive but more specifice), mucous membrane thickness > 5 - 6mm (sensitive but nonspecific)

What views can be done: Water’s view (maxillary sinusitis), Caldwell (ethmoid and frontal), Lateral (sphenoid), submentovertex (sphenoid and ethmoid)

What views should be done: Water’s view alone; add other views if Water’s is inconclusive or specifically looking for non-maxillary sinusitis

Overall 50% accurracy Xrays: false -ve in up to 40%, poor correlation with CT, sensitivities

reported range from 40 - 90% and specificity 75 - 100% but CT or MRI is used as gold standard which is problematic

Who should be Xrayed: if diagnosis uncertain but possible based on clinical criteria (2-3 out of 5 above criteria)

Be more aggressive with Xrays in looking for frontal sinusitis b/c of important consequences of rupture into CNS

Xrays in < 1yo not useful b/c of false opacification due to facial asymmetry and redundant mucosa

Axial or coronal CT Considered the radiological gold standard (A/F levels, sinus opacification,

sinus wall displacement, 4 mm or greater mucosal thickening) Need iv contrast to look for orbital or CNS complications CT is sensitive but lacks specificity thus CT findings need clinical

correlation (CT findings suggestive of sinusitis as incidental findings and in 84% of early cold symptoms)

Indications for CT: chronic sinusitis, suspected complication, failure of medical treatment

DIAGNOSIS Clinical diagnosis: definitive diagnosis is difficult No single symptom or sign is diagnostic Antral aspiration is gold standard: difficult, uncomfortable, maxillary only, not useful in ED Nasal and nasopharyngeal cultures correlate poorly with antrostomy cultures Culture and biopsy only for chronic and suspected fungal sinusitis Endoscopy of sinuses can be done Ultimately: clinical diagnosis; minimize testing as sensitivity and specificity are lacking Differential dx

Rhinits: increased response to deongestants, clear nasal discharge, absence of pain, no ostial obstruction and thus no facial pain

Tension headache, vascular headache, FB, dental disease, brain abscess, epidural abscess, meningitis, subdural empyema

Making the Diagnosis by History and Physical Examination: Williams 1992 Looked at various findings on hx and physical exam Note that sinusitis gold standard was defined radiographically (sinus

opacification, air - fluid level, mucous membrane > 6 mm thick)Symptom Sensitivity Specificity

- maxillary toothache 18 93- nonresponse to decongestants 41 80- hyposmia 56 64- colored discharge 72 52- myalgias 48 66- cough 70 44- preceeding URTI 50 61- headache 68 30- facial pain 52 43- painful chewing 13 84

Signs- purulent secretion 51 76- sinus tenderness 48 65- abnormal transillumination 73 54- temp > 38 16 83

CMAJ 1997: Likelihood of acute sinusitis as determined by number of signs and symptoms....

Symptom/Sign LR +veMaxillary toothache 2.5History of colored nasal secretion 1.5Poor response to decongestant 2.1Abnormal transillumination 1.6Purulent nasal secretion visualized 2.1

Number of findings0 0.11 0.52 1.13 2.64 6.4

Management based this­ 0 - 1: ruled out based on clinical features, no Xray­ 2 - 3: diagnosis unclear, sinus Xray recommended­ 4 - 5: actue bacterial sinusitis ruled in, no Xray

MANAGEMENT MOST will resolve spontaneously (60%), viral and bacterial Antibiotics

Antibiotics should be started if suspecting bacterial etiology Treatment approach similar to otitis media Amoxicillin X 10/7 is drug of choice (may be ineffective if B-lactamase

common): adequate coverage, best activity against penicillin intermediate B-lactam resistant pneumococcus, few side-effects, low resistance potential, no other antibiotic has been shown to be superior to amoxil in RCTs

Consider high dose amoxil for high risk children b/c of abx use w/i 3 months or day care (90 mg/kg/day tid instead of 40 mg/kg/day tid)

Penicillin allergic: trimethoprim - sulfamethoxazole, azithromicyin, cefuroxime

Rx failure after 7days: amoxicillin-clavulanate, cefuroxime, clindamycin, ciprofloxacin, clarithromycin, +/- flagyl

Chronic: cover B-lactamase and anaerobes Complications: iv abx, admission, ENT consultation

Decongestants /Adjuncts Reduces tissue edema, facilitates drainage, maintains patency of ostia NO good scientific evidence of effectiveness Topical and systemic should be used inconjunction Topical: phenylephrine 0.5%, oxymetazolin 0.05%; use for 3 - 5 days only

b/c extended use leads to rhinitis medicimentosa Oral: pseudoephrine, phenylpropanolamine (caution with TCA, MAO-I,

nonselective Beta-blockers) Antihistamines contraindicated unless allergic sinusitis (impedes sinus

drainage) Steroids for chronic and allergic sinusitis (controversial) Steam, humidifiers, nasal saline spray may help (indeterminate)

Disposition Most discharged home with oral abx Immunocompromised, severe co-morbid illness, toxic, poor follow up,

inability to tolerate po meds ----> admission for iv abx and observation Failure of definitive therapy means chronic sinusitis and ENT referral Frontal and sphenoid sinusitis with A/F levels may require hospitalization Fungal sinusitis requires admission, ENT consultation, iv antifungals,

surgical debridement —> watch for mucormyocosis which is aggressive and dangerous

RTED for severe headache, neurologic symptoms, visual changes ENT referral: > 4 episodes of bacterial sinusitis per year, chronic sinusitis,

anatomic abnormalities, complications

COMPLICATIONS Facial cellulits, periorbitral cellulitis, periorbital abscess, optic neuritis, blindneess, orbital

abscess Orbital complications: marked swelling, decreaed ocular motility, decreased visual acuity Intracranial: meningitis, cavernous sinus thrombosis, epidural or subdural empyema,

brain abscess; suspect with neuro s/s,

MISCELLANEOUSLINGULAR TONSILLITIS Rare cause of pharyngitis that usually occurs in patients who have had their palatine

tonsils removed Lingual tonsils are a collection oof nonencapsulated lymphoid tissue most commonly

located symmetrically on either side of the midline just below the inferior pole of the palatine tonsil and anterior to the vallecula at the base of the tongue

This lymphoid tissue may enlarge after puberty, repeated infections, tonsillectomy Sore throat that worsens with movement of tongue and phonation May have classic “hot potato” voice and complain of feeling a swelling in the throat Dysphagia, fever, resp distress, stridor may be present PE: normal appearing pharynx with mild hyperemia Laryngoscopy: edematous lingual tonsil covered with a purulent exudate Lateral neck Xray: normal epiglottis and aryepiglottic folds with a scalloped appearance

of the anterior surface of the vallecula caused by the enlarged tonsils Mx

Airway, abx, supportive AWO possible but rare Humidified oxygen, hydration, corticosteroids Nebulized epi for AWO may help Antibiotics as per pharyngitis

LARYNTITIS Hoarseness and aphonia Viral URTI Bacterial possible (strep, diptheria) TB, syphilis, leprosy, actinomyocosis, other fungal rare Consider epiglottitis Antibiotics only if suspecting bacterial

VIRAL RHINITIS > 100 viruses: rhinovirus, parinfluenza, RSV, etc Winter peak incidence Transmission via resp secretions Incubation 3 - 7 days Duration 3 - 7 days Antipyretics, nasal saline drops, humidified air, decongestants

ORAL ANGIOEDEMA: UVULITIS IgE mediated reaction characterized by edema of dermis especially in face/neck Non-pruritic, well-demarcated, localized, nonpitting edema of deep subcutaneous tissue

that primarily involves the periobital, perioral, intraoral regions CLUE: angioedema is NOT itchy Note: facial findings can be lateralized (one side only) Heriditary angioedema (HAE)

Autosomal dominant condition lacking C1 esterase inhibitor or functional

deficiency Cardinal s/s: edema of face, airway, or extremities, agdominal pain

associated with N/V/D Precipitated by trauma, stress Airway management is cornerstone of approach Acute management as per anaphylaxis although does not usually respond

well to epinephrine, antihistamines, or steroids FFP contains some C1 inhibitor; case reports of effectiveness C1 esterase concentrate replacement is probably the most important

treatment in a known HAE High dose epi may be effective

Acquired Angioedema ACE-I, NSAIDS, sulpha drugs, others Idiopathic is common Angioedema occurs with ACE - Is in 0.2% and can be at any time

(including years after onset); more common in blacks Mechanism: ? inhibition of bradykinin metabolism Management as above: consider FFP, d/c offending agent

Management Severe: treat as per anaphylaxis, intubate ASAP Moderate: treat as per anaphylaxis, watch airway closely Mild

­ Bendadryl­ Steroid X one dose­ Monitor 4-6hrs for progression